The synaptic cytoskeleton in development and disease

The synaptic cytoskeleton in development and disease
复制标题

DOI:
10.1002/dneu.20892
复制
发表时间:
2012-01-01
影响因子:
3
通讯作者:
Aberle, Hermann
Aberle, Hermann
中科院分区:
医学3区
文献类型:
--
作者:
Goellner, Bernd;Aberle, Hermann

文献摘要

被引文献

相似文献

细胞骨架形成神经元结构的骨架,维持其形状和大小、亚细胞区室和货物物流。突触的细胞骨架可以分为微管为基础的核心细胞骨架和皮层膜骨架。虽然中央微管形成了复杂的神经元过程,包括轴突和突触的建设的基本基础,皮质肌动蛋白丝通常被认为是突触动力学和可塑性的介质。最近,血影蛋白和锚蛋白分子的膜下网络已经参与了突触稳定性和维持的调节。突触细胞骨架的破坏主要影响突触的稳定性和成熟,但也其次干扰神经元通讯。因此,各种遗传性疾病都伴随着细胞骨架功能障碍,包括痉挛性截瘫、脊髓小脑共济失调和智力迟钝。由于许多这些疾病的主要原因仍然是未知的,具有保守的细胞骨架元件库的模式生物有助于理解潜在的生物学机制。果蝇突触的惊人技术和遗传可及性表明,在突触终末最终从其靶细胞分离之前,细胞骨架结构的丧失导致轴突运输缺陷、突触成熟缺陷和突触终扣的回缩,这表明类似的过程可能涉及人类神经元疾病。(c)2011 Wiley Periodicals,Inc.开发神经生物学72:111125,2012
The cytoskeleton forms the backbone of neuronal architecture, sustaining its form and size, subcellular compartments and cargo logistics. The synaptic cytoskeleton can be categorized in the microtubule-based core cytoskeleton and the cortical membrane skeleton. While central microtubules form the fundamental basis for the construction of elaborate neuronal processes, including axons and synapses, cortical actin filaments are generally considered to function as mediators of synapse dynamics and plasticity. More recently, the submembranous network of spectrin and ankyrin molecules has been involved in the regulation of synaptic stability and maintenance. Disruption of the synaptic cytoskeleton primarily affects the stability and maturation of synapses but also secondarily disturbs neuronal communication. Consequently, a variety of inherited diseases are accompanied by cytoskeletal malfunctions, including spastic paraplegias, spinocerebellar ataxias, and mental retardation. Since the primary reasons for many of these diseases are still unknown model organisms with a conserved repertoire of cytoskeletal elements help to understand the underlying biological mechanisms. The astonishing technical as well as genetic accessibility of synapses in Drosophila has shown that loss of the cytoskeletal architecture leads to axonal transport defects, synaptic maturation deficits, and retraction of synaptic boutons, before synaptic terminals finally detach from their target cells, suggesting that similar processes could be involved in human neuronal diseases. (c) 2011 Wiley Periodicals, Inc. Develop Neurobiol 72: 111125, 2012